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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 473712, 9 pages
Research Article

Production of Adenosine by Ectonucleotidases: A Key Factor in Tumor Immunoescape

1INSERM U866, 21078 Dijon, France
2Faculté de Médecine, Université de Bourgogne, 21079 Dijon, France
3Department of Medical Oncology, Centre Georges François Leclerc, 21000 Dijon, France

Received 18 May 2012; Accepted 3 July 2012

Academic Editor: Karen M. Dwyer

Copyright © 2012 François Ghiringhelli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It is now well known that tumor immunosurveillance contributes to the control of cancer growth. Many mechanisms can be used by cancer cells to avoid the antitumor immune response. One such mechanism relies on the capacity of cancer cells or more generally of the tumor microenvironment to generate adenosine, a major molecule involved in antitumor T cell response suppression. Adenosine is generated by the dephosphorylation of extracellular ATP released by dying tumor cells. The conversion of ATP into adenosine is mediated by ectonucleotidase molecules, namely, CD73 and CD39. These molecules are frequently expressed in the tumor bed by a wide range of cells including tumor cells, regulatory T cells, Th17 cells, myeloid cells, and stromal cells. Recent evidence suggests that targeting adenosine by inhibiting ectonucleotidases may restore the resident antitumor immune response or enhance the efficacy of antitumor therapies. This paper will underline the impact of adenosine and ectonucleotidases on the antitumor response.